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Lichen planus and hepatitis C virus
792 Brief communications by random genetic events, more lesions may express a fully malignant phenotype. REFERENCES 1. Templeton AC. Kaposi's sarcoma. Pathol Ann 1981;2:31536. 2. Reynolds WA, Winkleman RK, Soule EH. KS: a clinicopathologicstudy with particular reference to its relationship to the reticuloendothelial system. Medicine (alt), 1965;44: 419-43. 3. Cox PH, Helwig EG. Kaposi's sarcoma. Cancer 1959; 12:289-98. 4. Templeton AC. Studies in KS. Postmortem findings and disease pattern in women. Cancer 1972;30:854-67. 5. Zeigler JL, Dorfman RE. Kaposi's sarcoma: pathophysiology and conical management. New York: Marcel Dekker, 1988. 6. Redfield RR. The clinical, research, and public health applications of the WaIter Reed staging classification ofHIY infections. Third International Conferenceon AIDS. Washington DC M.11.1;8:1986. 7. Schwart RA, Kardashian JP, McNutt NS, et aI. Cutaneous angiosarcoma resembling KS in a homosexual man. Cancer 1983;51:721-6. 8. Enzinger PM, Weiss SW. Soft tissue tumors: St. Louis: CY Mosby, 1988;533-80. 9. Harawi S. Kaposi's sarcoma in: Harawi SI, O'Hara CJ, eds. Pathology and pathophysiology of AIDS and HIYrelated diseases. London: Chapman and Hall Ltd., 1989:83133.
Lichen planus and hepatitis C virus M. Mokni,a M. Rybojad,a D. Puppin, Jr.,a S. Catala,a F. Venezia,b RDjian,b and P. Morela Paris, Fraru:e The frequency and the specificity of a possible clinical relation betweenlichen planus (LP) and liver disease have been reviewed recently,l-4 A multicenter case control study5 showed that increased alanine aminotransferase and aspartate aminotransferase activities and a positive test for hepatitis B virus surface antigen approximately doubled the risk of lichen planus. In addition, the same study noted that the increased risk of LP in patients with liver disorders (high transaminase activities) is still significant after adjustment for the presence of hepatitis B virus surface antigen and a history of viral hepatitis. The authors suggested that there may be an indirect relation between LP and other hepatotropic viruses that are posFrom the Departments of Dermatology' and Gastro-enterology,b Saint-Louis Hospital. Reprint requests: Pro P. Morel, Clinique Dermatologique, Hopital Saint-Louis, 75475 Paris Cedex 10, France. 16/4/27455
Journal of the American Academy of Dermatology
sibly transmitted in a similar manner to hepatitis B virus such as non-A, non-B hepatitis, cytomegalovirus, and Epstein-Barr virus. We report a patient in whom LP developed during chronic hepatitis, probably in response to the hepatitis C virus (HCV). Case report. In 1980, a 33-year-old man addicted to heroin was found to have increased transaminase levels. These levels have persisted and have intermittently increased in value. In 1989 itchy, flat-topped violaceous papules appeared on the patient's arms and rapidly spread to the trunk. A biopsy specimen confirmed the diagnosis of LP. Values from laboratory studies in 1989 were as follows: aspartate aminotransferase, 102 U/L (normal 4 to 27 U/L; alanine aminotransferase, 50 U/L (normal 4 to 27 U/L); gammaglobulinemia, 13 gm/L (normal 11 to 15 gm/L); albuminemia, 47 gm/L (normal 40 gm/L). AntiHBc and anti-HCY tests (Ortho HCY ELISA) were positive. Antinuclear, antimitochondria, and anti-smooth muscle antibody tests were negative. Serologic tests for human immunodeficiency virus types 1 and 2 were also negative. A biopsy specimen of the liver was consistent with chronic active hepatitis.
Discussion. Our patient appears to have an HCVrelated hepatitis. Chronic hepatitis B can be excluded because, except for a positive anti-HBc antibody, all markers·of HBV infection were absent. The specificity of enzyme immunoassay for antibodies against HCV has been recently questioned in patients with autoimmune chronic active hepatitis and hypergammaglobulinemia. 6 However, these conditions were absent in our patient, who had none of the autoantibodies usually found in autoimmune hepatitis. He also had normal serum globulin and IgG concentrations. The occurrence of LP in a patient with HCV hepatitis may be coincidental. To our knowledge this is the first such observation reported. We would be interested to know the incidence of LP in HCV hepatitis. This might be achieved by examining drug addicts both prospectively and retrospectively because a large percentage of them are infected with HCV. REFERENCES 1. Rebora A, Rongioletti P. Lichen planus and chronic active hepatitis. A retrospective survey. Acta Derm Venereol (Stockh) 1984;64:52-6. 2. Mobacken H, Nilsson LA, Olsson R, et al. Incidence ofliver disease in chronic lichen planus of the mouth. Acta Derm Venereol (Stockh) 1984;64:70-3. 3. Monk BE. Lichen planus and the liver [Letter]. J AM ACAD DERMATOL 1985;12:122-3. 4. Korkij W, Chuang TY, Soltani K. Liver abnormalities in patients with lichen planus. A retrospective case-control study. J AM ACAD DERMATOL 1984;11:609-15. 5. Gruppo Italiano Studi Epidemiologici in Dermatologia (GISED). Lichen planus and liver diseases: a multicentric case-control study. Br Med J 1990;300:227-30. 6. McFarlane IG, Smith HM, Johnson PJ, et aI. Hepatitis C virus antibodies in chronic active hepatitis: pathogenic factor or false-positive result? Lancet 1990;335:754-7.
Lichen planus and hepatitis C virus M. Mokni,a M. Rybojad,a D. Puppin, Jr.,a S. Catala,a F. Venezia,b RDjian,b and P. Morela Paris, Fraru:e The frequency and the specificity of a possible clinical relation betweenlichen planus (LP) and liver disease have been reviewed recently,l-4 A multicenter case control study5 showed that increased alanine aminotransferase and aspartate aminotransferase activities and a positive test for hepatitis B virus surface antigen approximately doubled the risk of lichen planus. In addition, the same study noted that the increased risk of LP in patients with liver disorders (high transaminase activities) is still significant after adjustment for the presence of hepatitis B virus surface antigen and a history of viral hepatitis. The authors suggested that there may be an indirect relation between LP and other hepatotropic viruses that are posFrom the Departments of Dermatology' and Gastro-enterology,b Saint-Louis Hospital. Reprint requests: Pro P. Morel, Clinique Dermatologique, Hopital Saint-Louis, 75475 Paris Cedex 10, France. 16/4/27455
Journal of the American Academy of Dermatology
sibly transmitted in a similar manner to hepatitis B virus such as non-A, non-B hepatitis, cytomegalovirus, and Epstein-Barr virus. We report a patient in whom LP developed during chronic hepatitis, probably in response to the hepatitis C virus (HCV). Case report. In 1980, a 33-year-old man addicted to heroin was found to have increased transaminase levels. These levels have persisted and have intermittently increased in value. In 1989 itchy, flat-topped violaceous papules appeared on the patient's arms and rapidly spread to the trunk. A biopsy specimen confirmed the diagnosis of LP. Values from laboratory studies in 1989 were as follows: aspartate aminotransferase, 102 U/L (normal 4 to 27 U/L; alanine aminotransferase, 50 U/L (normal 4 to 27 U/L); gammaglobulinemia, 13 gm/L (normal 11 to 15 gm/L); albuminemia, 47 gm/L (normal 40 gm/L). AntiHBc and anti-HCY tests (Ortho HCY ELISA) were positive. Antinuclear, antimitochondria, and anti-smooth muscle antibody tests were negative. Serologic tests for human immunodeficiency virus types 1 and 2 were also negative. A biopsy specimen of the liver was consistent with chronic active hepatitis.
Discussion. Our patient appears to have an HCVrelated hepatitis. Chronic hepatitis B can be excluded because, except for a positive anti-HBc antibody, all markers·of HBV infection were absent. The specificity of enzyme immunoassay for antibodies against HCV has been recently questioned in patients with autoimmune chronic active hepatitis and hypergammaglobulinemia. 6 However, these conditions were absent in our patient, who had none of the autoantibodies usually found in autoimmune hepatitis. He also had normal serum globulin and IgG concentrations. The occurrence of LP in a patient with HCV hepatitis may be coincidental. To our knowledge this is the first such observation reported. We would be interested to know the incidence of LP in HCV hepatitis. This might be achieved by examining drug addicts both prospectively and retrospectively because a large percentage of them are infected with HCV. REFERENCES 1. Rebora A, Rongioletti P. Lichen planus and chronic active hepatitis. A retrospective survey. Acta Derm Venereol (Stockh) 1984;64:52-6. 2. Mobacken H, Nilsson LA, Olsson R, et al. Incidence ofliver disease in chronic lichen planus of the mouth. Acta Derm Venereol (Stockh) 1984;64:70-3. 3. Monk BE. Lichen planus and the liver [Letter]. J AM ACAD DERMATOL 1985;12:122-3. 4. Korkij W, Chuang TY, Soltani K. Liver abnormalities in patients with lichen planus. A retrospective case-control study. J AM ACAD DERMATOL 1984;11:609-15. 5. Gruppo Italiano Studi Epidemiologici in Dermatologia (GISED). Lichen planus and liver diseases: a multicentric case-control study. Br Med J 1990;300:227-30. 6. McFarlane IG, Smith HM, Johnson PJ, et aI. Hepatitis C virus antibodies in chronic active hepatitis: pathogenic factor or false-positive result? Lancet 1990;335:754-7.